Cardioprotective Effects of Cell Permeable NADPH oxidase inhibitors in Myocardial Ischemia/Reperfusion Injury

Issachar Devine; Qian Chen; Regina Ondrasik; William Chau; Katelyn Navitsky; On Say Lau; W. Parker; Kyle D. Bartol; B. Casey; Robert J. Barsotti; Lindon H. Young

Cardioprotective Effects of Cell Permeable NADPH oxidase inhibitors in Myocardial Ischemia/Reperfusion Injury

Issachar Devine
, Qian Chen
, Regina Ondrasik
, William Chau
, Katelyn Navitsky
, On Say Lau
, W. Parker
, Kyle D. Bartol
, B. Casey
, Robert J. Barsotti
, Lindon H. Young

Department of Bio-Medical Sciences (PCOM)

Research output: Other contribution

Abstract

During myocardial ischemia/reperfusion (I/R), the generation of reactive oxygen species (ROS) contributes to post-reperfused cardiac injury and contractile dysfunction. Activation of NADPH oxidase (NOX) during reperfusion generates ROS, and exacerbates I/R injury. We hypothesize that reducing ROS formation through inhibition of NOX will attenuate myocardial I/R injury in isolated perfused rat hearts subjected to I(30min)/R(45min) compared to untreated I/R hearts. The cell-permeable NOX inhibiting peptide, gp91 ds/tat (RKKRRQRRR-CSTRIRRQL-Amide, MW=2452 g/mol, 20μM, n=5), significantly improved post-reperfused cardiac function compared to controls (n=15, p

Original language	American English
State	Published - May 1 2013

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Cardioprotective Effects of Cell Permeable NADPH oxidase inhibitoFinal published version, 841 KBLicense: CC BY
Cardioprotective Effects of Cell Permeable NADPH oxidase inhibitoFinal published version, 841 KBLicense: CC BY

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title = "Cardioprotective Effects of Cell Permeable NADPH oxidase inhibitors in Myocardial Ischemia/Reperfusion Injury",

abstract = " During myocardial ischemia/reperfusion (I/R), the generation of reactive oxygen species (ROS) contributes to post-reperfused cardiac injury and contractile dysfunction. Activation of NADPH oxidase (NOX) during reperfusion generates ROS, and exacerbates I/R injury. We hypothesize that reducing ROS formation through inhibition of NOX will attenuate myocardial I/R injury in isolated perfused rat hearts subjected to I(30min)/R(45min) compared to untreated I/R hearts. The cell-permeable NOX inhibiting peptide, gp91 ds/tat (RKKRRQRRR-CSTRIRRQL-Amide, MW=2452 g/mol, 20μM, n=5), significantly improved post-reperfused cardiac function compared to controls (n=15, p",

author = "Issachar Devine and Qian Chen and Regina Ondrasik and William Chau and Katelyn Navitsky and Lau, \{On Say\} and W. Parker and Bartol, \{Kyle D.\} and B. Casey and Barsotti, \{Robert J.\} and Young, \{Lindon H.\}",

year = "2013",

month = may,

day = "1",

language = "American English",

type = "Other",

}

TY - GEN

T1 - Cardioprotective Effects of Cell Permeable NADPH oxidase inhibitors in Myocardial Ischemia/Reperfusion Injury

AU - Devine, Issachar

AU - Chen, Qian

AU - Ondrasik, Regina

AU - Chau, William

AU - Navitsky, Katelyn

AU - Lau, On Say

AU - Parker, W.

AU - Bartol, Kyle D.

AU - Casey, B.

AU - Barsotti, Robert J.

AU - Young, Lindon H.

PY - 2013/5/1

Y1 - 2013/5/1

N2 - During myocardial ischemia/reperfusion (I/R), the generation of reactive oxygen species (ROS) contributes to post-reperfused cardiac injury and contractile dysfunction. Activation of NADPH oxidase (NOX) during reperfusion generates ROS, and exacerbates I/R injury. We hypothesize that reducing ROS formation through inhibition of NOX will attenuate myocardial I/R injury in isolated perfused rat hearts subjected to I(30min)/R(45min) compared to untreated I/R hearts. The cell-permeable NOX inhibiting peptide, gp91 ds/tat (RKKRRQRRR-CSTRIRRQL-Amide, MW=2452 g/mol, 20μM, n=5), significantly improved post-reperfused cardiac function compared to controls (n=15, p

AB - During myocardial ischemia/reperfusion (I/R), the generation of reactive oxygen species (ROS) contributes to post-reperfused cardiac injury and contractile dysfunction. Activation of NADPH oxidase (NOX) during reperfusion generates ROS, and exacerbates I/R injury. We hypothesize that reducing ROS formation through inhibition of NOX will attenuate myocardial I/R injury in isolated perfused rat hearts subjected to I(30min)/R(45min) compared to untreated I/R hearts. The cell-permeable NOX inhibiting peptide, gp91 ds/tat (RKKRRQRRR-CSTRIRRQL-Amide, MW=2452 g/mol, 20μM, n=5), significantly improved post-reperfused cardiac function compared to controls (n=15, p

UR - https://digitalcommons.pcom.edu/research_day/research_day2013/research2013/28

M3 - Other contribution

ER -

Cardioprotective Effects of Cell Permeable NADPH oxidase inhibitors in Myocardial Ischemia/Reperfusion Injury

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